摘要:这3名患者在取得稳定的分子学缓解之后(融合基因转阴PCRU)停用达沙替尼。1名患者复发,另外两名患者在1年后仍保持了PCRU。以前说过,达沙替尼确实可以提高免疫力,希望今后能获得更多的相关研究报告。: c7 L2 w" h4 k: R5 [- p: U
关于这个研究值得注意的是,这三名患者都是服用格列卫失败后转用达沙替尼的,也即他们对格列卫是耐药的。这与法国的格列卫停药研究又有所不同,那个研究中的患者都是对格列卫反应良好的。希望医生们能扩大研究长期观察,看看停用达沙替尼是否能持久不复发。* s, {+ ] N! J2 I! x
/ ~* N7 S' [- F G: N作者:来自澳大利亚+ o( j* F# f9 s- u2 n
来源:Haematologica. 2011.8.9.
$ B; @/ n- C1 U! DDear Group,# }) i' j# b! U" C
/ ^ M2 L6 ]% Q. ESome of you are on Dasatinib (Sprycel) and we wish to give news on all CML
! G# G3 n5 `3 S7 dtherapies. Here is a report from Australia on 3 patients who went off Sprycel3 W0 b/ n/ \( o
after stable molecular response (PCRU). 1 patient relapsed but 2/3 patients) {( i& s' t( D( L( g; ]
remain in stable PCRU at the 1 year mark. Some of you may remember that Sprycel1 R4 { s, _: f4 l( B& c
does spike up the immune system so I hope more reports come out on this issue.5 ^& k4 }5 h8 a5 g8 \# j1 x
+ E, w5 X. J5 s5 [The remarkable news about Sprycel cessation is that all 3 patients had failed
: [ ] S5 g1 O# P. U2 B6 b* FGleevec and Sprycel was their second TKI so they had resistant disease. This is6 v& f1 b6 v/ z& o; o6 i
different from the stopping Gleevec trial in France which only targets patients& g0 z1 e; t l* L; p! z" S
who have done well on Gleevec.& `: i4 S! }+ [ h/ c
A4 E" z' c+ q. W6 p- N# LHopefully, the doctors will report on a larger study and long-term to see if the% T3 g: H% o1 w2 _+ K; s( u6 ]
response off Sprycel is sustained.- \: m7 Q; V2 X; n& q( q k$ u
! L: |$ F% D4 x k. A* W) z$ W* cBest Wishes," H; J& m/ ?, a3 F0 C# F# H- W
Anjana
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/ V$ C8 H" w. i# F# P sHaematologica. 2011 Aug 9. [Epub ahead of print] t; P! X8 o( i
Durable complete molecular remission of chronic myeloid leukemia following9 W# E7 v( V" L! O0 S d. w6 ~
dasatinib cessation, despite adverse disease features.
1 G( m+ B1 T! T2 t/ m7 \. x P2 hRoss DM, Bartley PA, Goyne J, Morley AA, Seymour JF, Grigg AP.( x/ [- e4 D, ~$ o+ ^- V) ?
Source
7 T& d, h/ e; J2 g1 W2 VAdelaide, Australia;: L- ~2 X; _: V4 N
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Abstract
! ]' w( v9 l( K5 k7 y; k( t7 ZPatients with chronic myeloid leukemia, treated with imatinib, who have a) I4 H. u1 i6 z9 J1 @8 @* e
durable complete molecular response might remain in CMR after stopping
5 S9 s* f' L3 W# d$ ]( m! Ktreatment. Previous reports of patients stopping treatment in complete molecular
0 u( F- M W$ aresponse have included only patients with a good response to imatinib. We$ D0 a2 T0 G+ i4 K3 w( N
describe three patients with stable complete molecular response on dasatinib
, S4 @+ O7 m1 N+ A* R0 ~* qtreatment following imatinib failure. Two of the three patients remain in
" F k. o$ v, [3 M) I) Xcomplete molecular response more than 12 months after stopping dasatinib. In
" g/ Y$ l: M8 E6 Pthese two patients we used highly sensitive patient-specific BCR-ABL1 DNA PCR to
9 ] t. d7 Q7 T+ Kshow that the leukemic clone remains detectable, as we have previously shown in
0 R$ }" y! Z2 z: s; x% gimatinib-treated patients. Dasatinib-associated immunological phenomena, such as
/ V# r9 T5 v. S2 k5 ^/ [" gthe emergence of clonal T cell populations, were observed both in one patient" a: a. g' l0 l5 g$ Y$ x p8 m
who relapsed and in one patient in remission. Our results suggest that the
* b$ `6 Z% B, C2 S8 c0 Z5 o2 ~+ lcharacteristics of complete molecular response on dasatinib treatment may be8 m/ M. e! R- H$ @, n' _0 ?* j
similar to that achieved with imatinib, at least in patients with adverse8 k G8 f5 |$ t2 D( T/ t
disease features.
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